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Considering this, CVB infection, particularly persistent infection, may contribute to the overall demise of the cell population by further activating autoreactive T cells, augmenting the effects of autoimmunity, and by further inducing cell stress and death

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Proposed mechanisms include enhanced insulinotropic activity, improved adipose tissue handling of nutrients, central effects on appetite and reward pathways, and improved tolerability or pharmacodynamic balance when combined with GLP-1 receptor agonism